Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease characterized by an increase in ventricular mass in the absence of another cause for cardiac hypertrophy. Approximately 15% of familial cases are caused by one of more than 37 distinct point mutations in the Beta myosin heavy chain (BMHC) gene. This gene has been shown to be expressed in slow skeletal muscle fibers as well as in the heart. Myosin extracted from skeletal muscle of these HCM patients demonstrates abnormal function in a variety of in vitro assays. Furthermore, histological examination of these biopsies reveals the presence of skeletal muscle hypertrophy and the absence of mitochondria from the center of many of the type-I fibers, a pattern resembling central-core disease. Studies in other labs have shown that primary cultures of normal animal skeletal myoblasts undergo hypertrophy when subjected to an alternating electrical field. Myocytes expressing the BMHC gene mutations are predisposed to hypertrophy in the patient. Thus, it should be possible to study the molecular concomitants of hypertrophy induced by an electrical field in myoblasts from normal individuals as well as in myoblasts obtained from HCM patients with identified BMHC mutations.